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- ALS (1)
- Alzheimer's Disease (1)
- As those identified in primary tauopathies (e.g. P301L and G389R) (1)
- Both enhanced vesicular release of tau in the extracellular space (1)
- Drosophila (1)
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- Due to a process called phase separation. My Thesis tested the hypothesis that tau mutations (1)
- In both HEK293T and SHSY-5Y cells compared to wild type. However (1)
- Into either HEK293T (1)
- It has recently been well accepted that tau is also an intrinsically disordered protein that tends to form membraneless organelles called coacervates (1)
- Might impair the phase separation properties of the protein and impact its pathological role in cells. I first tested the effect of single amino acid substitutions in vitro (1)
- Mitochondrial dysfunction (1)
- Motor neuron disease (1)
- Neurodegeneration (1)
- Neuromuscular junction (1)
- One third is characterized by the presence of genetic mutations leading to the synthesis of tau proteins with single amino acid substitutions at specific locations and affecting protein function. While most of the initial studies have emphasize the functional role of tau as modulator of the axonal cytoskeleton (1)
- Optogenetics (1)
- Or in SHSY-5Y neuroblastoma cells (1)
- Phase Separation (1)
- SecretionTau is a protein expressed exclusively in glia and neurons in the central nervous system and implicated in several neurogenerative diseases called “tauopathies”. Among all the tauopathies (1)
- Tau (1)
- The expression of tau mutants did not affect cell viability in response to oxidative stress. While the relationship between the biophysical properties of tau and its function in cells remain to be elucidated (1)
- This study suggest potential mechanisms by which specific mutations of tau may induce its release in the extracellular space and suggest a potential role in spreading of the pathology. (1)
- Using recombinant tau and the results revealed that the tau pathogenic mutations P301L and G389R increased the propensity of tau to phase separate and form coacervates with higher viscosity than wild type. I then hypothesized that tau mutants and wild type tau may also differentially impact cell function. This was studied by transfecting tau and its two mutants P301L and G389R (1)
- Via calcium-dependent membrane blebbing (1)
- We determined that tau P301L and G389R (1)
- We used a bimolecular fluorescence complementation assay based on the formation of tau dimers fused with either the N or C terminus of the reporter VENUS fluorescent protein. Using live imaging (1)
- Which do not express endogenous tau (1)
- Which endogenously express tau. For the experiments (1)
Articles 1 - 2 of 2
Full-Text Articles in Genetics and Genomics
Characterization Of Pathological Tau Mutants, Charles J. Mcdonald
Characterization Of Pathological Tau Mutants, Charles J. Mcdonald
Dissertations, Theses, and Capstone Projects
Tau is a protein expressed exclusively in glia and neurons in the central nervous system and implicated in several neurogenerative diseases called “tauopathies”. Among all the tauopathies, one third is characterized by the presence of genetic mutations leading to the synthesis of tau proteins with single amino acid substitutions at specific locations and affecting protein function. While most of the initial studies have emphasize the functional role of tau as modulator of the axonal cytoskeleton, it has recently been well accepted that tau is also an intrinsically disordered protein that tends to form membraneless organelles called coacervates, due to a …
Validating A New In Vivo Model To Study Als, Izabela J. Cimachowska
Validating A New In Vivo Model To Study Als, Izabela J. Cimachowska
Student Theses and Dissertations
Buildup of oxidative stress and mitochondrial dysfunction are well known characteristics of both sporadic and hereditary amyotrophic lateral sclerosis (ALS). While both forms of the disease seem to arise from common cellular dysfunction, the genetic disease is studied to a much greater extent. Engineering novel animal models of the sporadic form of the disease is crucial for development of druggable targets to treat ALS and understand the underlying mechanisms. Interestingly, accumulation of oxidative stress by exacerbated emission of reactive oxygen species (ROS) from presynaptic mitochondria is a hallmark of both hereditary and sporadic ALS. Previous work by our laboratory showed …